Endometrial leukocytes are altered numerically and functionally in women with implantation defects.
OBJECTIVE
A significant cohort of women with autoimmune thyroid disease (ATD) also suffer from reduced fertility. The finding that neither exogenous hormones nor donor eggs correct the infertility suggests that the problem involves an inherent endometrial defect.


METHODS
Endometrial leukocyte populations in women with ATD were quantitated by immunohistochemistry. A semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) technique was used to examine the expression of transforming growth factor (TGF)-beta 1, interleukin (IL)-4, IL-10, and interferon (IFN)-gamma in the endometrial samples.


RESULTS
A significant increase in the endometrial T-cell population was observed in women with ATD compared to controls. The relative abundance of IL-4 and IL-10 was decreased in women with ATD compared to controls, whereas IFN-gamma was increased. No difference was noted in the abundance of TGF-beta 1. The source of cytokine production for IL-4, IL-10, and IFN-gamma was the endometrial leukocytes.


CONCLUSIONS
Both the leukocyte numbers and cytokine expression profile were altered significantly in a well-defined group of women with implantation defects.
Stewart-Akers
A M
AM
Magee-Womens Research Institute, University of Pittsburgh, PA, USA.
Krasnow
J S
JS
Brekosky
J
J
DeLoia
J A
JA
D001327:Autoimmune Diseases / Q000150:complications* / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis; D010064:Embryo Implantation; D004717:Endometrium / Q000166:cytology* / Q000378:metabolism; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications* / Q000473:pathology; D007037:Hypothyroidism / Q000150:complications* / Q000473:pathology; D007150:Immunohistochemistry; D007247:Infertility, Female / Q000209:etiology*; D007962:Leukocytes / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D016133:Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D013959:Thyroid Diseases / Q000150:complications* / Q000276:immunology / Q000473:pathology; D014158:Transcription, Genetic
D016207:Cytokines; D000949:Histocompatibility Antigens Class II